Mitochondrial health, the epigenome and healthspan
Open accessAbstract
Food nutrients and metabolic supply-demand dynamics constitute environmental factors that interact with our genome influencing health and disease states. These gene-environment interactions converge at the metabolic-epigenome-genome axis to regulate gene expression and phenotypic outcomes. Mounting evidence indicates that nutrients and lifestyle strongly influence genome-metabolic functional interactions determining disease via altered epigenetic regulation. The mitochondrial network is a central player of the metabolic-epigenome-genome axis, regulating the level of key metabolites [NAD(+), AcCoA (acetyl CoA), ATP] acting as substrates/cofactors for acetyl transferases, kinases (e.g. protein kinase A) and deacetylases (e.g. sirtuins, SIRTs). The chromatin, an assembly of DNA and nucleoproteins, regulates the transcriptional process, acting at the epigenomic interface between metabolism and the genome. Within this framework, we review existing evidence showing that preservation of mitochondrial network function is directly involved in decreasing the rate of damage accumulation thus slowing aging and improving healthspan.
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Metabolic networks, in particular those in the mitochondria, directly transmit information about the cells metabolic state to epigenetic programming enzymes.
“Metabolic networks, in particular those in the mitochondria, directly transmit information about the cells metabolic state to epigenetic programming enzymes that, for instance, add or remove epigenetic markers onto chromatin (128, 129).”
From Metabolic Flexibility as an Adaptation to Energy Resources and Requirements in Health and Disease (2018) · cites this paper as [129]
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- Authors
- Aon, M. A., Cortassa, S., Juhaszova, M., & Sollott, S. J.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Cortassa, Sonia
- Juhaszova, Magdalena
- Venue
- Clinical Science
- Publisher
- Portland Press Ltd.
- Published
- 2016-06-29
- Volume
- 130
- Issue
- 15
- Pages
- 1285-1305
- ISSN
- 0143-5221 (ISSN-L)
- 1470-8736
- PMC
- PMC5066813
- OpenAlex
- W2466333622
- Cited by
- 66
- References
- 237
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 4 · 2023: 7 · 2022: 6 · 2021: 7 · 2020: 8 · 2019: 5 · 2018: 6 · 2017: 8 · 2016: 3
- FWCI
- 0.66
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (Z99 AG999999)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Keywords
- mitochondrial health, epigenome, healthspan, aging, gene-environment interaction, chromatin regulation, sirtuins, NAD+, acetyl-CoA, protein acetylation, deacetylase, protein kinase A, nutrient metabolism, lifestyle, damage accumulation
- MeSH terms
- Adolescent, Adult, Age Factors, Aged, Aged, 80 and over, Aging, Animals, Child, Child, Preschool, DNA, Mitochondrial, Energy Metabolism, Gene Expression Regulation, Health Status, Humans, Infant, Infant, Newborn, Life Style, Longevity, Middle Aged, Mitochondria, Mutation, Nutritional Status, Genome, Human, Epigenesis, Genetic, Young Adult, Gene-Environment Interaction
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